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INT-1B3 miR-193a-3p mimic boosts t cell immunity and induces tumor cell death

Proposed mode of action of INT-1B3/1B3.INT-1B3/1B3 induces apoptosis and cell death leading to expression of DAMPs, e.g., expression of calreticulin, reduced expression of CD39 and CD73 and thus reduced levels of ATP. Release of DAMPs induces maturation of DC and these DC can activate CD4+, CD8+ and CD4-CD8- T cells upon stimulation. Activated CD4+, CD8+ and CD4-CD8- T cells produce IFNγ, TNFα and granzyme B which leads to cytotoxicity against tumor cells. This illustration was created with https://www.biorender.com/. Credit: 2024 Duurland et al.

A research paper has been published in Oncotarget titled, "INT-1B3, an LNP formulated miR-193a-3p mimic, promotes anti-tumor immunity by enhancing T cell mediated immune responses via modulation of the tumor microenvironment and induction of immunogenic cell death."

In this study, Chantal L. Duurland and others from InteRNA Technologies BV, Utrecht, The Netherlands, and Crown Bioscience Inc., in San Diego, examined the effect of their lipid nanoparticle (LNP) formulated, chemically modified, synthetic miR-193a-3p mimic (INT-1B3) on anti-tumor immunity.

"In this study, we examined the effect of our lipid nanoparticle (LNP) formulated, chemically modified, synthetic miR-193a-3p mimic (INT-1B3) on animal survival, tumor microenvironment (TME) and induction of anti-tumor immune responses," say the authors.

The study demonstrates for the first time that miR-193a-3p induces long-term immunity against tumor development via modulation of the tumor microenvironment and induction of immunogenic cell death.

Additionally, the data show that systemic administration of INT-1B3 to 4T1 and H22 tumor bearing immunocompetent mice prolonged animal survival by reducing metastasis compared to phosphate buffered saline (PBS) or anti-programmed death (PD) 1 treatment.

More information: Chantal L. Duurland et al, INT-1B3, an LNP formulated miR-193a-3p mimic, promotes anti-tumor immunity by enhancing T cell mediated immune responses via modulation of the tumor microenvironment and induction of immunogenic cell death, Oncotarget (2024). DOI: 10.18632/oncotarget.28608

Journal information: Oncotarget 

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